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PubMed1994

Alterations of local cerebral glucose utilization in lean and obese fa/fa rats after acute adrenalectomy.

An animal model often used to investigate the aetiology of obesity is the genetically obese fa/fa rat. It has many abnormalities, including hyperphagia, hyper-insulinemia, insulin resistance, low cerebral glucose utilization and an overactive hypothalamo-pituitary adrenal (HPA) axis with resulting hypercorticism. Due to the latter consideration, the aim of this work was to study the impact of acute adrenalectomy (ADX) on the local cerebral glucose utilization (LCGU) of lean and obese fa/fa rats. ADX resulted in discrete increases in LCGU of regions common to both lean and obese rats. These common regions were found to belong to be related to the limbic system. Within this system, the LCGU of the brain of obese rats was either normalized to lean sham operated values or increased by ADX to a similar degree in both groups on a percentage basis. It was concluded that the LCGU of both lean and obese animals appears to be negatively regulated, albeit to different extents, by glucocorticoids. Such negative regulation is particularly salient within the limbic system of the lean rat and even more so in the fa/fa rat. It is suggested that the long-term hypercorticism of obese fa/fa rats due to abnormal regulation of the HPA axis may result in a decreased LCGU in limbic and related regions of the brain of fa/fa rats and contribute to the expression of the obese phenotype.

Adrenalectomy↗
PubMed1994

Effects of adrenalectomy and type I or type II glucocorticoid receptor activation on 5-HT1A and 5-HT2 receptor binding and 5-HT transporter mRNA expression in rat brain.

We evaluated the effects of adrenalectomy (ADX) and replacement with glucocorticoid receptor agonists on serotonin (5-HT) 5-HT1A and 5-HT2 receptor binding in rat brain. 5-HT1A receptor binding was increased in the CA2-CA4 and the dentate gyrus of the hippocampus 1 week after ADX. This effect was prevented by the systemic administration of aldosterone (10 micrograms/microliters/h) but not by RU28362 (10 micrograms/microliters/h). No significant effect was observed on 5-HT2 receptor binding in rat cortex. The expression of 5-HT transporter mRNA was unchanged in the raphe nucleus as measured by in situ hybridization.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

Effects of adrenalectomy and corticosterone replacement on glucocorticoid receptor levels in rat brain tissue: a comparison between western blotting and receptor binding assays.

A sensitive Western blotting technique, using a commercially available antibody, was developed herein to study glucocorticoid receptor (GR) autoregulation in brain tissue. A prominent immunoreactive band at approximately 94 kDa, representing the GR, was observed in soluble fractions prepared from rat hippocampus whereas two bands (approximately 97 and 94 kDa) were detected in frontal cortex preparations. Four-day adrenalectomy significantly increased immunoreactive GR levels in both brain regions. In contrast, adrenalectomized animals implanted with corticosterone pellets of varying concentrations displayed dose-dependent decreases in immunodetectable GR levels. Radioligand binding assays ([3H]dexamethasone +/- RU 28362), performed on these same tissue preparations, revealed a similar pattern of GR response to that measured by Western blotting. However, changes in GR binding capacity were generally greater in magnitude than corresponding changes in immunoreactive GR levels. This discrepancy was most pronounced in adrenalectomized animals administered a bolus of corticosterone 1 h prior to sacrifice where a 60-70% reduction in receptor binding sites occurred, in sharp contrast to the 25-30% decrease in immunoreactive GR levels. Taken together, our findings suggest that Western blotting can be used to study GR regulation in brain tissue and that changes in steroid-binding capacity may not necessarily reflect changes in receptor protein levels.

Adrenalectomy↗
PubMed1995

Region-specific alterations of calbindin-D28k immunoreactivity in the rat hippocampus following adrenalectomy and corticosterone treatment.

The aim of this study was (i) to compare the immunocytochemical distribution of the calcium-binding protein calbindin-D28k (CB) in the hippocampus of rats with the pattern of neurodegeneration following adrenalectomy (ADX) using silver impregnation, and (ii) to investigate the CB-immunoreactivity in the hippocampus following 3 weeks corticosterone treatment. 24 h following ADX no degenerative changes, nor alterations in CB-immunoreactivity were found in the hippocampus. Both 3 and 21 days following ADX neurodegeneration in the dentate gyrus could be observed which was accompanied with a loss of CB-immunoreactive (CB-ir) cells in that parts of the dentate gyrus suffering neuronal degeneration. Additionally we observed a marked loss of CB-ir in the CA1 area both 3 and 21 days following ADX. Three weeks daily corticosterone treatment (10 mg/day) induced a marked increase of CB-ir exclusively in the CA1 pyramidal cell layer. We conclude that (i) there is a close relationship between the loss of CB-immunoreactive cells in the DG and the neuronal degeneration in the dentate gyrus following ADX, and (ii) corticosterone appears to be involved in the regulation of calbindin-D28k in the CA1 pyramidal cell layer.

Adrenalectomy↗
PubMed1983

Effect of adrenalectomy and demedullation of the adrenals on vasopressor responses to stimulation of postjunctional alpha 2-adrenoceptors.

After adrenalectomy performed 18-12 h previously, the vasopressor responses induced by stimulation of postjunctional alpha 2-adrenoceptors (agonist: B-HT 920) were attenuated in pithed normotensive rats in contrast to pressor responses mediated by postjunctional alpha 1-adrenoceptors (agonist: cirazoline). Aldosterone and desoxycorticosterone both enhanced the vasopressor responses to the alpha 2-adrenoceptor agonist B-HT 920 in adrenalectomized rats, but did not fully restore the effects. Demedullation of the adrenals also attenuated the vasoconstrictor processes evoked by stimulation of postjunctional alpha 2-adrenoceptors 18-22 h later. This effect was reversed after an infusion with adrenaline. The combination of aldosterone and adrenaline produced full recovery of the increase in diastolic pressure elicited via alpha 2-adrenoceptors in adrenalectomized (18-22 h) animals. The results suggest that circulating adrenaline and aldosterone (or corticosterone) are required for optimal functioning of vascular postjunctional alpha 2-adrenoceptors.

Adrenal Cortex Hormones↗
PubMed1984

Naloxone inhibits both glucocorticoid and [D-Ala2,Met5]enkephalinamide reversal of behavioural effect of adrenalectomy.

Intact rats treated immediately after a 15-min swimming exposure with i.m. 1 or 10 mg/kg naloxone (but not with 10 mg/kg of MRZ2593, a quaternary analogue) showed significant reduction in immobility (55, 30%) compared with controls (70%) during a 5-min retest 24 h later. This effect of naloxone was seen when administered 1 h prior to retest. Adrenalectomized rats, as previously shown, are only approximately 30% immobile on retest; administration of [D-Ala2,Met5]enkephalinamide (50 micrograms i.m.) or dexamethasome (6 micrograms i.m.) elevated immobility to 66 and 69% respectively. Administration of naloxone (0.1-10 mg/kg) progressively antagonized the effect of both [D-Ala2,Met5]enkephalinamide and dexamethasone, to 36 and 41% immobility on retest at 10 mg/kg. We conclude that the incorporation of information post-stress normally involves at least two opioidergic pathways, and that the integrity of one of these pathways is an absolute requirement for such incorporation to occur, based on the naloxone studies. In contrast, either glucocorticoids or enkephalin analogues are sufficient to restore behaviour post-adrenalectomy, suggesting that corticosteroid-dependent neural mechanisms may substitute for this second opioidergic pathway.

Adrenalectomy↗
PubMed1985

A kappa-selective opioidergic pathway is involved in the reversal of a behavioural effect of adrenalectomy.

We have shown previously that adrenalectomized rats are immobile for only approximately 30% of a 5 min retest period, 24 h after an initial 15 min swimming exposure, compared with approximately 70% immobility for intact animals. The administration of ketocyclazocine, dynorphin-(1-17) or [Met5]enkephalin[Arg6,Phe7] immediately after initial exposure reversed the effect of adrenalectomy, whereas equimolar doses of morphine sulphate, [D-Ala2,D-Leu5]enkephalin and dynorphin-(1-8) were inactive. MR2266, a kappa-selective partial agonist/predominant antagonist, did not reverse immobility but antagonized the reversing effect of ketocyclazocine. In conjunction with our previous studies, we interpret these data to show that one of the opioidergic pathways for the incorporation of information post-stress is kappa-selective. This kappa selectivity in turn suggests a possible physiological role for prodynorphin-derived peptides in memory.

Adrenalectomy↗
PubMed1989

Effects of adrenalectomy on responses mediated by dopamine D-1 and D-2 receptors.

The effects of surgical adrenalectomy were investigated on behavioural responses produced by the selective D-1 agonist, SK&F 38393, alone, and in combination with the D-2 agonist, quinpirole (LY171555). Further, stereotyped responses to apomorphine and LY171555 were assessed following treatment with either the D-1 or the D-2 antagonists, SCH 23390 and raclopride, respectively. There was no difference between sham-adrenalectomized (sham) and adrenalectomized (ADX) groups in responses to SK&F 38393. Although concomitant stimulation of both receptor subtypes increased the incidence of stereotyped sniffing behaviour, there was no difference in the magnitude of this effect between the sham and ADX groups. Raclopride reduced LY171555-induced sniffing and hypothermia less in ADX rats than in sham controls, which was consistent with the hypothesis that adrenocortical hormones affect D-2 receptor responsiveness. SCH 23390 had a greater inhibitory effect on LY171555 responses, but a smaller effect on apomorphine responses in the ADX group compared with their sham controls. It is concluded that the amplified D-2-stimulated response observed in ADX rats may be more dependent on tonic D-1 receptor activation than the control D-2 response of shams.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1991

Adrenalectomy, but not vagotomy, reverses the worsening effect of Ca2+ blockers on ethanol-induced gastric lesions in rats.

This study examines the influence of the adrenals and of the vagus nerve on the lesion-worsening action of nitrendipine or verapamil on 75% ethanol-induced gastric mucosal damage in rats. Bilateral adrenalectomy antagonized ethanol lesion aggravation by nitrendipine or verapamil; instead, dose-related lesion reduction was seen. Dexamethasone treatment of adrenalectomized rats restored the lesion-enhancing effects of both Ca2+ channel blockers. Bilateral subdiaphragmatic vagotomy failed to abolish the adverse action of nitrendipine or verapamil on ethanol lesions. The findings suggest that the adrenal corticoids modulate the worsening effect of Ca2+ channel antagonists on ethanol-induced gastric damage; when the influence of the adrenal steroids is removed, these compounds become gastroprotective.

Adrenalectomy↗
PubMed1994

Adrenalectomy does not modify the suppressive effect of angiotensin II on voluntary ethanol drinking in rats.

Enhancement of activity in the renin-angiotensin system reduces voluntary ethanol consumption in rats. Because angiotensin II, which is a major bioactive component of the renin-angiotensin system, stimulates the release of aldosterone, aldosterone may play a role in the reduction of ethanol intake by angiotensin II. The present study examined ethanol drinking in a group of rats that was bilaterally adrenalectomized and incapable of producing aldosterone, and in a sham group that underwent similar surgery except that the adrenal glands were left intact. Rats were maintained on ad libitum food, water and 1.5% saline solution in their home cages. Access to ethanol (6% weight/volume) was restricted to a daily 40 min period and was always offered as a choice in conjunction with water. Adrenalectomy did not alter the effect of angiotensin II on ethanol intake as subcutaneous injections of angiotensin II (400 micrograms/kg) significantly reduced ethanol intake to the same degree in both the adrenalectomized and sham groups. In the next phase, daily subcutaneous injections of aldosterone (100 micrograms/kg) reduced the home cage intake of 1.5% saline in the adrenalectomized group indicating that this dose of aldosterone was biologically active. These aldosterone injections did not affect ethanol intake in either the adrenalectomized or sham groups. Under the present conditions of testing aldosterone does not appear to play a role in the angiotensin II-induced reduction of ethanol consumption.

Adrenalectomy↗
PubMed1983

Early adrenalectomy stimulates subsequent growth and development of the rat brain.

Rats were adrenalectomized (ADX) or sham-operated (SHAM) on the 11th day of life and subsequent brain development (cerebrum and cerebellum) studied in terms of tissue weight and biochemical composition. Measured at about 65 days of age, early ADX subjects had significantly heavier brains (in terms of both wet and dry weights) than SHAMs, despite being lighter in overall body weight. Brain protein and DNA contents were elevated, as was the activity of 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP), a myelin marker enzyme. Glycerol-3-phosphate dehydrogenase (GPDH), a glucocorticoid-regulated enzyme, was reduced in activity. Although both the cerebrum and cerebellum showed the growth-enhancing effects of early adrenalectomy, the DNA and CNP changes were most pronounced in the cerebrum. Finally, the effect of adrenal removal on myelinogenesis was confirmed by subcellular fractionation experiments demonstrating that more myelin could be recovered from the brains of ADX than from SHAM animals. These results are significant in terms of the influence of adrenal secretions on normal brain development and the role of GPDH in myelin lipid biosynthesis.

Adrenalectomy↗
PubMed1989

Neonatal adrenalectomy alters dendritic branching of hippocampal granule cells.

Alterations in glucocorticoid hormones are known to affect the development of brain and behavior, but the details of these effects at the cellular level are unclear. The present study was undertaken to determine whether dendritic growth and branching in glucocorticoid target neurons, the granule neurons of the hippocampal dentate gyrus, are affected by glucocorticoid hormones. Computerized morphometric analysis of Golgi impregnated granule cells showed that adrenalectomy on Postnatal Day 21 resulted in a small decrease in dendritic branching of lower order dendrites in both male and female rats at 42 days of age, while branching of distal dendrites was left unaffected. Conversely, dendritic branching in rats treated daily with hydrocortisone acetate (5 mg/kg) during the same period was not significantly different from that of untreated rats. Total dendritic length was unaffected by either treatment. These results suggest that relatively minor alterations may occur in the circuitry in the inner molecular layer of the dentate gyrus, a region involving intrahippocampal connections, in the absence of physiological levels of glucocorticoid hormones. Whether these effects are mediated via glucocorticoid hormone effects on the presynaptic afferent neurons or via granule cell metabolic pathways remains to be determined. The most surprising result, given the presence of glucocorticoid receptors in granule cells and the relatively dramatic effects of glucocorticoid manipulations on whole brain that have been reported, is that the effects of these manipulations on dendritic morphology are minimal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1991

Long-term adrenalectomy causes loss of dentate gyrus and pyramidal neurons in the adult hippocampus.

A growing literature suggests that the hippocampus can be damaged by glucocorticoids, the adrenal steroids secreted during stress. Thus, considerable interest was generated by recent reports that prolonged elimination of glucocorticoids by adrenalectomy (ADX) damages hippocampal dentate gyrus neurons. To date, this phenomenon has only been observed in rats of peripubertal age or younger; moreover, reports differ considerably as to the magnitude of the damage induced. Therefore, we examined this issue in rats ADXd at 5 months of age. Three months later, there was a significant 26% loss of dentate neurons in a subset of rats. In agreement with these previous reports, this subset had attenuated weight gain and electrolyte imbalances, suggestive of complete removal of the adrenals and accessory adrenal tissue. As a novel observation, we also observed significant (19%) loss of CA4 pyramidal neurons. Thus, both severe under- or overexposure to glucocorticoids can be deleterious to a number of hippocampal neuron types.

Adrenal Cortex Hormones↗
PubMed1991

Effect of chronic adrenalectomy on neuron loss and distribution of sulfated glycoprotein-2 in the dentate gyrus of prepubertal rats.

This study extends the unexpected finding of Sloviter et al. (Science, 1989, 243: 535-538) that adrenalectomy (ADX) of young rats casues a loss of granule neurons in the dentate gyrus. In particular, we determined how the vulnerability of dentate granule neurons to the cytocidal effect of ADX is related to the completeness of the ADX and whether sulfated glycoprotein-2, a putative component of programmed cell death, is associated with the death of granule neurons after ADX. We report that 4 months after bilateral ADX of young (150-175 g) rats only ADX rats that had attenuated weight gain and less than 2 ng/ml of serum corticosterone lost granule neurons; whereas as little as 15 ng/ml of serum corticosterone was sufficient to protect granule neurons from cell death. In addition, by immunocytochemistry, SGP-2 was distributed as punctate deposits throughout the molecular layer of the dentate gyrus and in glial cells juxtaposed to surviving neurons in the dentate of ADX rats with a granule cell loss. However, immunoreactivity for SGP-2 was not found in granule neurons that exhibited morphological signs of cellular generation after ADX.

Adrenal Glands↗
PubMed1984

Sexual behavior of male rats: influence of short- and long-term adrenalectomy.

Adult male rats (3 months old) were tested for their copulatory behavior: those satisfying the criterion of sexual vigor in the last three out of five weekly tests were randomly divided into two groups and adrenalectomized or sham operated, and their copulatory activity was retested 35 and 420 days after surgery. Short-term adrenalectomy did not modify any of the parameters of sexual behavior. On the other hand, a higher percentage of adrenalectomized than of sham-operated rats still had successful sexual performance when 18 months old (420 days after surgery); moreover, blood levels of testosterone were higher in adrenalectomized than in sham-operated old rats. The possibility that adrenal steroids may play a role in the age-linked decline in male sexual activity in mammals is discussed.

Adrenal Glands↗
PubMed1994

The response of brown adipose tissue mitochondrial glycerolphosphate acyltransferase to cold-exposure in hypothyroidism, after adrenalectomy and after treatment with cycloheximide.

1. Exposure to cold has previously been shown to considerably increase the activity of the mitochondrial form of glycerolphosphate acyltransferase (GPAT) in brown adipose tissue (A. C. Darnley, C. A. Carpenter and E. D Saggerson, Biochem. J. 253, 351-355, 1988; J. R. D. Mitchell and E. D. Saggerson. Biochem. J. 277, 665-669, 1991). 2. Both adrenalectomy and chemically-induced hypothyroidism increased mitochondrial GPAT activity in rats maintained at 21 degrees C. This increase was similar to that caused by exposing rats to the cold (4 degrees C) for three days. Whereas exposure of hypothyroid rats to cold (4 degrees C) resulted in a further increase in GPAT activity, no further increase in activity was observed after exposure of adrenalectomized rats to the cold. 3. Administration of triiodothyronine (T3) to rats maintained at 21 degrees C had no effect on mitochondrial GPAT activity. 4. Prior treatment with cycloheximide abolished 60-70% of the increase in GPAT activity caused by cold-exposure.

Acclimatization↗
PubMedDate not supplied

Cholestyramine feeding in weaned rats. Increase in plasma corticosterone levels and bile acid synthesis following adrenalectomy.

Feeding cholestyramine to weaned rats increased the bile acid pool and activity of cholesterol 7 alpha-hydroxylase as expected. Following adrenalectomy, cholestyramine still increased the activity of cholesterol 7 alpha-hydroxylase but the magnitude of increase was lower (P less than 0.01) than noted in intact rats. Surprisingly, cholestyramine feeding to both intact and adrenalectomized rats increased plasma levels of corticosterone.

Adrenal Glands↗